A Case of Pulmonary Embolism; Medical Student’s Experience

By: Muhamad Na’im B. Ab Razak Medical student of University Science of Malaysia

Case Summary 53 Years Old Malay Lady who was recently discharge from ward with problem list of morbid obesity, uncontrolled diabetes mellitus, hyperlipidaemia and hypertension presented to emergency department with the chief complaint of sudden onset severe shortness of breath associated with central pleuritic chest pain and diffuse sweating. She was alert and oriented to the time, place and person. Her blood pressure was 180/88 mmHg, heart rate was 120 b.p.m and respiratory rate was 20 breath per minute. Full blood count, Renal Function Test were inconclusive. Cardiac biomarkers were not elevated, D Dimer was >5000 ng/ml. ECG shows classical feature of Pulmonary embolism which are tachycardia, Deep S wave in lead I, Deep Q wave in lead III and inverted T wave in lead III (S1Q3T3) ABG under high flow mask of 100% oxygen, 10 L/min showed pH of 7.4, PCO2 28.6 mmHg, PO2 131 mmHg,HCO3

- 19.6 mmol/L. Calculated Alveolar-arterial gradient (A-a gradient) was 190 which suggestive of V/Q mismatch. A diagnosis of Pulmonary embolism was made based on high index of suspiciousness in risk factor, clinical presentation, ECG

findings and A-a gradient. Therefore, CT Angiography was done and showed feature of extensive pulmonary embolism. IV streptokinase 250 000 unit stat was commenced and followed with Streptokinase IV infusion 500 000 unit in 50 ml normal saline and patient was transferred to Cardiology Care Unit for further management.

Fig 1: Urgent CTA of thorax shows good opacification of pulmonary trunk but inhomogenous opacification of bilateral right and left main pulmonary artery with filling defect seeing within. Radiological diagnosis of pulmonary embolism was made by radiologist.

Discussion. Pulmonary embolism (PE) is not a disease per se but often a complication of other vascular problem particularly deep vein thrombosis. The devastating consequence of this disease is mainly resulting from the difficulty in establishing the diagnosis nonspecific signs and symptoms. Mortality in untreated PE is approximately 30%, but with adequate (anticoagulant) treatment, this can be reduced to 2Torbicki et al] PE occurs when when one or more pulmonary artery being blocked by blood clots that dislodged from peripheral veinthe blockage occurs at the bifurcation of the main pulmonary artery, then it is called saddle pulmonary embolism The blockake cause V/Q mismatch in which the lung tissue is ventilated but not perfused. This will give rise to intrapulmonary dead space and impair gas exchange. After hours,

Fig 2: ECG shows Tachycardia, Deep S wave in lead I, Deep Q wave i

is not a disease per se but often a complication of other vascular problem particularly deep vein

ing consequence of this disease is mainly resulting from the

establishing the diagnosis due to .

Mortality in untreated PE is approximately (anticoagulant)

to 2–8%. [A.

one or more pulmonary artery being blocked by blood

dislodged from peripheral vein. If the blockage occurs at the bifurcation of the main pulmonary artery, then it is called

The blockake cause V/Q mismatch in which the lung tissue is ventilated but not perfused. This will give rise to intrapulmonary dead

After hours,

this non perfused lung will no longer secretes surfactant and cause alcollapse which exacerbates the hypoxemia. The non perfused lung tissue however seldom become infarcted because of continuous oxygen supply by bronchial circulation and airways. The European Society of Cardiologyclassified PE into two main groups which are massive and non-massive. Mconsists of shock and/or(defined as a systolic blood pressuremmHg or a pressure drop of >15 min if not caused by newarrhythmia, hypovolumia Otherwise non-massive PE can bediagnosed. In other words, massive PE also defined as embolus causing sufficient obstruction topulmonary flow to result in hemodynamic instability, right ventricular failure, and hypoxemia [Paul Maggio et al]

ECG shows Tachycardia, Deep S wave in lead I, Deep Q wave in lead III and inverted T wave in lead III (S1Q3T3)

this non perfused lung will no longer secretes surfactant and cause alveolar collapse which exacerbates the hypoxemia. The non perfused lung tissue however seldom become infarcted because of continuous oxygen supply by bronchial

European Society of Cardiology has classified PE into two main groups which

massive. Massive PE consists of shock and/or hypotension (defined as a systolic blood pressure <90 mmHg or a pressure drop of 40 mmHg for >15 min if not caused by new-onset

volumia or sepsis). massive PE can be

In other words, massive PE also defined as embolus causing sufficient obstruction to pulmonary flow to result in hemodynamic instability, right ventricular failure, and

et al]

n lead III and inverted T

Virchow’s triad consist of stasis of the blood, hypercoagulable state and endothelial damage has been attributed to the deep vein thrombosis and PE. This condition can be due to blood and blood vessel disorder, prolong immobilization, prolong surgery, pregnancy, oral contraceptive and estrogen replacement, and malignancy. Even though the signs and symptoms for PE are not specific, Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) study found out that the most common presentation are dyspnea (73%), pleuritic chest pain (66%), cough (37%), and hemoptysis (13%) [Nader Kamangar]. Other atypical symptoms include seizure, syncope, abdominal pain, fever, productive cough, wheezing, altered sensorium, new onset atrial fibrillation, and flank pain. In a time without or not readily accessible CT angiography, few scoring system has been develop to predict the possibility of PE with the famous scoring system being Geneva score and Wells score. However, both of this scoring system has not been validated and derived from selected population. Therefore, diagnosis of PE should be made based on high level of suspiciousness in the presence of risk factor and clinical manifestation. Chest X Ray is not really help in detecting PE but it may show Westermark sign, Hamptom Hump and pulmonary effusion. However, it is good to rule out other causes of dyspnoe.

Wells score for Probability of PE

Criteria Points Clinical signs of DVT +3 Alternative diagnosis less probable than PE

+3

Heart rate > 100 b.p.m +1.5 Immobilization or surgery < 4 Weeks ago

+1.5

Previous DVT or PE +1.5 Haemoptysis +1 Cancer +1 Table 1: Total score: <2 indicates a low probability of PE;

2–6 indicates a moderate probability of PE; >6 indicates a

high probability of PE

ECG is a poor diagnostic tool for PE and it is rather being used to rule out other potential life threatening diagnosis such as myocardial infarction. [Chan TC et al]. The ECG is often abnormal in PE however, the findings are not sensitive and not specific. [Chan TC et al]. T-wave inversion in the precordial leads is the most common abnormality (68%), and represents the ECG sign best correlated to the severity of the PE.[Emile Ferrari et al]. In the same study, Emile Ferrari et al found out that Anterior T wave inversions had a sensitivity of 85% and specificity of 81% for massive PE. The so called classical ECG manifestation of PE which is the SI Q3 T3 pattern was described by McGinn and White in the year of 1935. However, it is not a pattern that characterize the pulmonary embolism alone but rather sign of acute cor pulmonale. Therefore, other causes giving rise to cor pulmonale such as acute bronchospasm and pneumothorax may as well give this ECG pattern. Apart from that, ECG findings often shows tachycardia.

D Dimer is a degradation product of crosslinked fibrin. Previously, it is being used as one of the main screening investigation for PE. However, it has less positive prediction value in diagnosing PE. A level of D- Dimer below than 500 µg . l-1

is a cut off point to safely excludes PE. There is a practice among the clinician to calculate alveolar-arterial gradient in order to establish the diagnosis of PE. This value, can be calculated based on ABG result using the below formula. Normal adult A-a gradient is 20. However, Marc A. Rodger et al found out that none of the ABG data or prediction rules had sufficient negative predictive value, specificity, or likelihood ratios to be useful in the management of patients with suspected PE. Therefore, they conclude that ABG data alone or in combination with other clinical data are not useful in the assessment of suspected PE.

A-a gradient = PAO2 − PaO2

[FiO2*(Patm-PH2O)-(PaCO2/0.8) ] - PaO2 PAO2 = alveolar PO2 (calculated from the alveolar gas equation) PaO2 = arterial PO2 (measured in arterial blood A-a gradient) = ( 760 - 47 ) x FiO2 - PaCO2 /0.8 (or 1)

Table 2 A-a gradient

Echocardiography may suggest or reinforce clinical suspicion of PE if right ventricular (RV) overload and dysfunction is found in the presence of Doppler signs of increased

pulmonary arterial pressure. A typical echocardiographic picture of haemodynamically significant PE includes dilated, hypokinetic RV, an increased RV/LV ratio caused by interventricular septal bulging into the LV, dilated proximal pulmonary arteries, increased velocity of the jet of tricuspid regurgitation (usually in the range of 3–3·5 m s-1), and disturbed flow velocity pattern in the RV outflow tract. Furthermore, the inferior vena cava is usually dilated and does not collapse on inspiration. [A. Torbicki et al] The gold standard for diagnosing pulmonary embolism is CT Angiography. CT has become the first-line modality for imaging in patients suspected of having PE. CT is now an attractive means for establishing a safe, highly accurate, and cost-effective diagnosis of PE. [U.J Schoepf & P. Costello]. However, according to cohort study by M. J. L. Van Strijen et al, the sensitivity of spiral CT was 86% for segmental or larger PE and 21% in the group of patients with subsegmental PE. Therefore, they draw a conclusion that in patients with clinically suspected PE and an abnormal perfusion scintigraphy, single-slice detector spiral CT is not sensitive enough to be used as the sole test to exclude PE. Doppler ultrasound is both 95% sensitive and specific in detecting deep venous thrombosis above the knee if DVT is suspected as causes of PE.

In the recent guidelines of the American College of Chest Physicians, either LMWH or UFH is recommended for the initial treatment of venous thromboembolism. In patients with advanced renal insufficiency, the recommendation is to use UFH rather the LMWH. [GF Pineo& RD Hull]. Vitamin K antagonists (VKAs) are the agents of choice for long-term treatment and secondary prophylaxis of pulmonary embolism (PE), as they were shown to be effective in preventing recurrence of the disease [G Agnelli & C Becattini]

Besides thrombolytic therapy, other management includes, high flow oxygen supply, continuous vital sign monitoring particularly SPO2, heart rate and BP, measures to prevent or control the effect of acute circulatory failure like infusion of Dobutamine and dopamine. The usefulness of fluid challenge is controversial and should not exceed 500 ml. as it may deteriorate the condition of the patient. Acute pulmonary thrombectomy has a limited role in massive, life-threatening PE.

Reference

1) A. Torbicki, E. J. R. van Beek , B. Charbonnier et al, "Guidelines on diagnosis and management of acute pulmonary embolism", European Heart Journal (2000) 21, 1301–1336

2) Chan TC, Vilke GM, et al. Electrocardiographic manifestations: pulmonary embolism. J Emerg Med. 2001; 21(3):263-70.

3) Emile Ferrari, Alain Imbert, Thierry Chevalier, et al, "The ECG in Pulmonary Embolism : Predictive Value of Negative T Waves in Precordial Leads--80 Case Reports", Chest 1997;111;537-543

4) Marc A. Rodger, Marc Carrier, Gwynne N. Jones et al, " Diagnostic Value of Arterial Blood Gas Measurement in Suspected Pulmonary Embolism ", Am. J. Respir. Crit. Care Med., Volume 162, Number 6, December 2000, 2105-2108

5) M. J. L. Van Strijen, W. De Monye, G. J. Kieft et al, "Accuracy of single-detector spiral CT in the diagnosis of pulmonary embolism: a prospective multicenter cohort study of consecutive patients with abnormal perfusion scintigraphy", Jour of Thromb and Haem, Vol 3, Issue 1, pages 17-25, International Society on Thrombosis and Haemostasis, 2010

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10) U. Joseph Schoepf & Philip Costello, " CT Angiography for Diagnosis of Pulmonary Embolism: State of the Art", Radiology, Volume 230, Number 2, 2004